CD40L启动CD4^＋T细胞缺乏小鼠免疫反应的研究

随着HIV感染者及各类医疗措施导致的免疫受损者的增多，探讨一种适合免疫缺陷人群的预防机会感染的策略越来越受到重视。研究表明，CD4^＋T细胞是抵抗肺孢子菌等机会感染的最主要因素，但不是唯一的因素。其中CD40配体（CD40L）被认为是一种可以启动B细胞和CD8^＋T细胞反应的关键因子。为探讨CD4^＋L是否能在缺乏CD4^＋T细胞的小鼠体内启动免疫反应，本文研究了用卵白蛋白（OVA）作为模型抗原，联合应用CD40L引起的免疫反应。结果显示，同时应用OVA和CD40L，可使CD4^＋T细胞耗竭小鼠体内抗OVA IgG抗体和抗原特异性IFN明显增多，提示在CD4^＋T细胞缺乏的宿主体内，CIMOL可以启动B细胞和CD8^＋T细胞类免疫反应。该结果为抗肺孢子菌等机会性感染的免疫预防研究提供可贵的资料。

CD40L priming the immune response in mice lacking CD4+ T cells

Since the increasing populations of HW-infected and immune-compromised patients due to immunosuppressive medical regimens, there was need to develop CD4^＋ T cell-independent therapeutic strategies to prevent opportunistic infection. There was a well-known inverse relationship between CD4^＋ lymphocyte count and the risk ofpneumocystis infection and other bacterial infection,but the CD4^＋ T cells does not hold all of the answers to mechanisms of host defense against these infections. CD40 ligand （CD4OL） was critical for host defense against pneumocystis as well as other opportunistic infections. To test whether CD40L could prime immune response in the deficiency of CD4^＋ T cells in mice, chicken ovalbumin （OVA） was used as the model antigen with the addition of CD40L in CD4-depleted mice. Anti-OVA IgG1 and IgG2a were measured by ELISA three weeks after the boost. The result showed significant increases in IgG2a and IgG1 in the CD40L co-transduced group compared to OVA alone. We also observed a significant increase in OVA-specific IFN-γ elaboration in splenocytes after stimulation with the SIINFEKL peptide in both CD4-replete mice and CD4-depleted mice that were co-transduced with CD40L. These data suggest that CD40L can prime both B-cell and CD8^＋ T-cell responses.